Lecture Notes Chapter 9: Smoke Inhalation

Injury and Burns

Objectives §  List the factors that influence mortality rate § Describe the nature of smoke inhalation and the

fire environment § Recognize the pulmonary and systemic

changes that occur following smoke inhalation and burn injury

§  List the effects of smoke inhalation injury on the upper and lower airways

§  Identify methods to diagnose smoke inhalation injury and CO poisoning

Objectives § Describe the methods used to determine the

type and extent of burn injury § Recognize the emergent treatment for smoke

inhalation injury and CO poisoning § Describe the airway and ventilatory support

strategies for smoke inhalation and burn injury § Describe the fluid, surgical, and nutritional

support used in the treatment of burn injuries

Introduction §  Fire is a major source of injury, death, and

economic loss §  Burns rank third most common cause of serious

injury and death §  80% of deaths in residential fires §  5%–10% mortality due to asphyxiation, systemic

poisoning, and respiratory tract injury

Introduction §  Prevalence of smoke inhalation among burn

victims = 10%–35% §  Pulmonary complications according to the

resuscitative phase §  Early (first 24 hours)

§  Inhalation of toxic or hot gases § Fluid loss § Heavy sedation

Introduction §  Intermediate (2–7 days) post resuscitative

phase §  Analgesic-related respiratory dysfunction §  Secretion retention §  Airway obstruction §  Atelectasis §  ARDS

Introduction §  Late (> 7 days)

§  Pneumonia §  Sepsis §  Multiple organ dysfunction §  Pulmonary embolism §  Chronic pulmonary disease

Etiology §  Fire – residential fires – most common §  Superheated gases §  Scalding liquids § Chemicals §  Electrical currents

Pathophysiology: Early Pulmonary and Systemic Changes § Within 24 hours post-burn

§  Carbon monoxide § Produced in fire environment, especially if

§ Oxygen levels are low § Combustion is incomplete

§ Rapidly absorbs into blood

Pathophysiology: Early Pulmonary and Systemic Changes § Carbon monoxide

§  It converts HbO2 into HbCO § Normal HbCO: < 3% § Minor smoke inhalation: 10%–15% § Severe smoke inhalation: > 50%

§  Compromise of O2 transport §  Inability of Hb to transport O2

§  The Hb conversion and inhibition of O2 release result in Functional anemia

Pathophysiology: Early Pulmonary and Systemic Changes § Carbon monoxide

§  Skeletal and cardiac muscle dysfunction §  Cerebral vasodilation §  Rapid loss of consciousness and cerebral edema §  Lethal CO poisoning typically occurs when COHb

> 50%–60%

Pathophysiology: Early Pulmonary and Systemic Changes § Hydrogen cyanide (HCN)

§  Linked to early and late death in burned patients §  Easily transported to tissues through circulatory

system; blocks tissue use of O2 §  Shift to anaerobic metabolism and elevated lactic

acid production

Pathophysiology: Early Pulmonary and Systemic Changes § Other considerations

Reduced oxygen transport Cellular metabolic dysfunction

Release of inflammatory mediators Vascular changes

Compromise of nervous system, cardiovascular

system, and skeletal muscle function (Causes of death)

Pathophysiology: Early Pulmonary and Systemic Changes § Other considerations

§  Thermal injury to the respiratory tract § Typically confined to the face, oral and nasal

cavities, pharynx, and trachea § Blistering, edema, accumulation of thick saliva,

and glottic closure if severe

Pathophysiology: Early Pulmonary and Systemic Changes § Other considerations

§  Chemical injury to the respiratory tract §  Injuries extend into the lungs § Tracheobronchitis, bronchospasm, bronchorrhea,

mucosal sloughing, airway obstruction § Alveolar de-recruitment - atelectasis § Pulmonary edema in severe cases

Pathophysiology: Early Pulmonary and Systemic Changes § Other considerations

§  Systemic changes are associated with § Decline in O2 transport § Metabolic derangement § Release of inflammatory mediators § Fluid loss

Pathophysiology: Intermediate Pulmonary and Systemic § Changes (2–7 days post-burn)

§  Signs of respiratory distress often after 24–48 hours

§  PVR returns to normal §  Hypermetabolic state continues

§  Increased O2 consumption and CO2 production

Pathophysiology §  Airway edema resolves between day 2 and 4 §  Increased mucus production §  Atelectasis, pleural effusion, acute lung injury

Pathophysiology: Late Pulmonary and Systemic Changes

§  > 7 days post-burn §  Hypermetabolic state for 1–3 wks §  Infection is the most common complication in this

period § Staphylococcus aureus § MRSA § Pseudomona aeruginosa

§  Pulmonary embolism can develop within 2 weeks of burn injury

Clinical Features §  Brain and heart = first to show dysfunction § HbCO content is potential indicator of the dose

of smoked inhaled §  SpO2 should not be used since HbO2 and

HbCO have similar light absorption

Clinical Features § Upper respiratory manifestations

§  Stridor – Hoarseness §  Difficulty speaking – Chest retractions

§  Severe form of inhalation injury §  Cough – Dyspnea §  Tachypnea – Cyanosis §  Wheezing – Crackles §  Rhonchi

Clinical Features: Chest Radiograph §  Frequently no signs in early period § CT scans may be more useful to determine

severity of pulmonary injury

Clinical Features: Arterial Blood Gases §  To trend the patient’s pulmonary insult § Reduced PaO2 and SaO2 § Reduced PaO2/FiO2 (ALI vs ARDS) § Respiratory alkalosis in early post-burn period § Metabolic acidosis and respiratory failure are

signs of life threatening injuries

Clinical Features: Hemodynamic Monitoring §  To optimize fluid resuscitation § Monitor

§  CVP §  PAP §  CO §  Urine output

Treatment § Goals of respiratory care in burn patient

§  Achieve a patent airway §  Secretion removal §  Maintenance of effective ventilation §  Preservation of lung volume §  Adequate oxygenation §  Maintenance of acid–base balance

Treatment: Airway § Monitor for airway closure § High Fowler’s position to reduce WOB §  Intubation if airway closure is anticipated §  Extubation if

§  Patient is improving §  Maintain his/her own secretions §  Cuff leak §  Adequate ventilation

Treatment: Carbon Monoxide Poisoning § Oxygen therapy: cornerstone of therapy (NRM) § High-flow mask CPAP 5–10 cm H2O if

§  Patient with minimal upper airway thermal injury §  Increasing dyspnea §  Increasing hypoxemia

§  Intubation if HbCO > 30%

Treatment § Mechanical Ventilation if

§  Respiratory failure §  Pneumonia §  ALI/ARDS §  Sedation and paralysis are necessary

Treatment: Fluid Balance §  To minimize development of

§  Shock §  Renal failure §  Pulmonary edema

Treatment: Prevention of Burn Complications §  Isolation technique § Room pressurization Front line of §  Air filtration infection defense § Wound covering §  Topical silver sulfadiazine §  Prophylactic antibiotics